Exercise-induced decreases in the 1 H transverse relaxation rate (R 2 ) of muscle have been well documented, but the mechanism remains unclear. In this study, the hypothesis was tested that R 2 decreases could be explained by pH decreases and apparent intracellular volume (V i ) increases. 31 P and 1 H spectroscopy, biexponential R 2 analysis, and imaging were performed prior to and following fatiguing exercise in iodoacetate-treated (IAA, to inhibit glycolysis), NaCN-treated (to inhibit oxidative phosphorylation), and untreated frog gastrocnemii. In all exercised muscles, the apparent intracellular R 2 (R 2i ) and pH decreased, while intracellular osmolytes and V i increased. These effects were larger in NaCN-treated and untreated muscles than in IAAtreated muscles. Multiple regression analysis showed that pH and V i changes explain 70% of the R 2i variance. Separate experiments in unexercised muscles demonstrated causal relationships between pH and R 2i and between V i and R 2i . These data indicate that the R 2 change of exercise is primarily an intracellular phenomenon caused by the accumulation of the end-products of anaerobic metabolism. In the NaCN-treated and untreated muscles, the R 2i change increased as field strength increased, suggesting a role for pH-modulated chemical exchange. Key words: skeletal muscle; exercise; hydrogen-ion concentration; osmolarity; nuclear magnetic resonance Exercise-induced increases in the apparent 1 H transverse relaxation time (T 2 ) of muscle water have been well documented. The amount of T 2 change increases as exercise intensity increases; T 2 plateaus 3-4 min after the onset of exercise (1). Following isometric leg extension to fatigue, T 2 recovery follows an approximately exponential time course and is complete after ϳ35 min. (2). The increase in signal intensity from active muscles in T 2 -weighted images allows muscle activity to be detected reliably and noninvasively, which may aid in the placement of regions of interest or surface coils in spectroscopic studies (2,3). With a full understanding of the mechanism(s) of the T 2 change, this phenomenon may also be useful in functional studies of muscle activation during exercise (e.g., Refs. 4 -6), noninvasive studies of pathologic conditions in which the T 2 response to exercise is altered (e.g., Refs. 7 and 8), and as a means of studying noninvasively those physiological changes that increase T 2 .The most universally offered and best-studied explanation for the T 2 increase during exercise is the concomitant increase in muscle volume. However, the mechanism of the T 2 increase is more complex than total water accumulation. For example, recovery of the muscle's anatomical cross-sectional area is faster than T 2 recovery (2), and enhancement of the extracellular fluid volume increase during exercise is not proportional to the T 2 increase (9). A further complication is that both ex vivo amphibian (10) and in vivo mammalian (11) studies suggest that exchange between the intra-and extracellular spaces in muscle is sl...

Extract of rat musclc tissue was shown to stimulate the incorporation of labclled sulphatc into embryonie chick cartilage. This stimulatory activity could still be demonstrated in the presencc of optimal concentrations of amino acids in the incubation medium. After passage of the musc\e extract through Sephadex the biological activity was found in a low molccular weight fractio? The addition of human growth hormone to rat muscle In vitra incrcased the stimulating activity of the extract.

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Injured adult tendons heal fibrotically and possess high re-injury rates, whereas fetal tendons appear to heal scarlessly. However, knowledge of fetal tendon wound healing is limited due in part to the need for an accessible animal model. Here, we developed and characterized an in vivo and ex vivo chick embryo tendon model to study fetal tendon healing. In both models, injury sites filled rapidly with cells and extracellular matrix during healing, with wound closure occurring faster in vivo. Tendons injured at an earlier embryonic stage improved mechanical properties to levels similar to non-injured controls, whereas tendons injured at a later embryonic stage did not. Expression levels of tendon phenotype markers, collagens, collagen crosslinking regulators, matrix metalloproteinases, and pro-inflammatory mediators exhibited embryonic stage-dependent trends during healing. Apoptosis occurred during healing, but ex vivo tendons exhibited higher levels of apoptosis than tendons in vivo. Future studies will use these in vivo and ex vivo chick embryo tendon injury models to elucidate mechanisms of stage-specific fetal tendon healing to inform the development of therapeutic approaches to regeneratively heal adult tendons.